Steroidogenesis in the adrenal gland occurs via highly related and controlled cytochrom P450 enzymes. Inhibition of Aldosterone Synthase or the enzyme cytochrom P450 11B2 (CYP11B2) represents a new pharmacological strategy to reduce excessive aldosterone levels. Aldosterone is a mineralocorticoid that is mainly synthesized in the adrenal gland and released into the circulation to control in the renal epithelium the sodium/potassium balance and thus water homeostasis and blood pressure as well as the in non-epithelial tissue of heart and kidney the formation of extracellular matrix and organ remodeling. Aldosterone synthase mediates in the adrenal gland the terminal and rate-limiting conversion of 11-deoxycorticosterone to corticosterone via 11-beta-hydroxylation, the conversion of corticosterone to 18-hydroxy-corticosterone via 18-methylhydroxylation and finally the conversion of 18-hydroxy-corticosterone to aldosterone via 18-methyloxidation. The activity and expression of the enzyme is mainly regulated by angiotensin II, potassium and adrenocorticotropin. These regulators of aldosterone synthase are sensitive to the actions of aldosterone and the physiological circadian rhythm and as such create an endocrine feedback loop. Angiotensin II is produced upon stimulation of renin activity that is triggered via sodium loss and blood pressure decrease due to hypoaldosteronemic states. Potassium is retained in exchange to sodium loss in hypoaldosteronemic conditions. Finally, adrenocorticotropin is produced from the pituitary gland in response to low glucocorticoid levels and the circadian rhythm. Hence, a selective inhibition of aldosterone synthase and a reduction of aldosterone secretion is counteracted with the stimulation of renin and the generation of angiotensin II as well as by a retention of potassium; both increased angiotensin II and potassium levels being potent stimulators of aldosterone synthase activity and thus aldosterone secretion. The circadian rhythm upon aldosterone synthase inhibition is blunted for aldosterone yet adrenocorticotropin levels are not significantly changed as glucocorticoids are the main regulators of adrenocorticotropin secretion. The rate-limiting enzyme of cortisol secretion is the adrenal enzyme 11-beta-hydroxylase or cytochrom P450 11B1 (CYP11B1) that converts 11-deoxycortisol to cortisol. Cortisol levels are controlled via the hypothalamic-pituitary-adrenal feedback loop by controlling the release of adrenocorticotropin (ACTH). Adrenocorticoptropin stimulates in the adrenal gland the early and late steroidogenic reactions leading to the synthesis of cortisol but also dehydroepiandrosterone and androstendione (see FIG. 1, a diagram for adrenal steroidogenesis). The cortisol-producing enzyme CYP11B1 shows a high sequence homology of 95% at the amino acid level to the aldosterone-producing enzyme CYP11B2. Therefore, a compound targeted at aldosterone synthase to reduce excessive aldosterone secretion needs to be tested for its enzyme selectivity.